Abstract

Cancer develops when cells no longer follow their normal pattern
of controlled growth. In the absence or disregard of such
regulation, resulting from changes in their genetic makeup, these
errant cells acquire a growth advantage, expanding into
precancerous clones. Over the last decade, many studies have
revealed the relevance of genomic mutation in this process, be it
by misreplication, environmental damage, or a deficiency in
repairing endogenous and exogenous damage. Here, we discuss
homologous recombination as another mechanism that can result in
a loss of heterozygosity or genetic rearrangements. Some of these
genetic alterations may play a primary role in carcinogenesis, but
they are more likely to be involved in secondary and subsequent
steps of carcinogenesis by which recessive oncogenic mutations are
revealed. Patients, whose cells display an increased frequency of
recombination, also have an elevated frequency of cancer, further
supporting the link between recombination and carcinogenesis.